Journal articles: 'SALT II'

1

HULETT, LOUISA S. "Carter, Salt II and Detente II." Australian Journal of Politics & History 28, no. 2 (April 7, 2008): 190–200. http://dx.doi.org/10.1111/j.1467-8497.1982.tb00177.x.

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Sartori, Leo. "Will SALT II Survive?" International Security 10, no. 3 (1985): 147. http://dx.doi.org/10.2307/2538945.

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Earle, Ralph. "Don't abandon SALT II." Bulletin of the Atomic Scientists 42, no. 7 (August 1986): 8–9. http://dx.doi.org/10.1080/00963402.1986.11459397.

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4

Mancini, Matthew. "Elvira Santamaria, Salt Cartographies II." Public 30, no. 59 (June 1, 2019): 204–6. http://dx.doi.org/10.1386/public.30.59.204_5.

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Mancini, Matthew. "Elvira Santamaria, Salt Cartographies II." Public 31, no. 59 (June 1, 2019): 204–6. http://dx.doi.org/10.1386/public.31.59.204_5.

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6

Rudd, M. Audrey, Maria Trolliet, Susan Hope, Anne Ward Scribner, Geraldine Daumerie, George Toolan, Timothy Cloutier, and Joseph Loscalzo. "Salt-induced hypertension in Dahl salt-resistant and salt-sensitive rats with NOS II inhibition." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 2 (August 1, 1999): H732—H739. http://dx.doi.org/10.1152/ajpheart.1999.277.2.h732.

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Although recent evidence suggests that reduced nitric oxide (NO) production may be involved in salt-induced hypertension, the specific NO synthase (NOS) responsible for the conveyance of salt sensitivity remains unknown. To determine the role of inducible NOS (NOS II) in salt-induced hypertension, we treated Dahl salt-resistant (DR) rats with the selective NOS II inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) for 12 days. Tail-cuff systolic blood pressures rose 29 ± 6 and 42 ± 8 mmHg in DR rats given 150 and 300 nmol AMT/h, respectively ( P < 0.01, 2-way ANOVA) after 7 days of 8% NaCl diet. We observed similar results with two other potent selective NOS II inhibitors, S-ethylisourea (EIT) and N-[3-(aminomethyl)benzyl]acetamidine hydrochloride (1400W). Additionally, AMT effects were independent of alterations in endothelial function as assessed by diameter change of mesenteric arterioles in response to methacholine using videomicroscopy. We, therefore, conclude from these data that NOS II is important in salt-induced hypertension.

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Nugraha, Yuda Prasetya, Haruki Sugiyama, and Hidehiro Uekusa. "Ciprofloxacin salt and salt co-crystal with dihydroxybenzoic acids." Acta Crystallographica Section E Crystallographic Communications 78, no. 3 (February 3, 2022): 259–63. http://dx.doi.org/10.1107/s2056989022001177.

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The crystal structure of two multi-component crystals of ciprofloxacin [systematic name: 1-cyclopropyl-6-fluoro-4-oxo-7-(piperazin-1-yl)quinoline-3-carboxylic acid], a fluoroquinolone antibiotic, namely, ciprofloxacin 2,6-dihydroxybenzoate salt, C17H19FN3O3 +·C7H5O4 −, (I), and ciprofloxacin hydrochloride–3,5-dihydroxybenzoic–water (1/1/1), C17H19FN3O3 +·Cl−·C7H6O4·H2O, (II), were determined. In (I) and (II), the ciprofloxacin cations are connected via head-to-tail N—H...O hydrogen bonding. Both structures show an alternating layered arrangement between ciprofloxacin and dihydroxybenzoic acid.

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8

Ando, K., Y. Sato, and T. Fujita. "Salt sensitivity in hypertensive rats with angiotensin II administration." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 5 (November 1, 1990): R1012—R1016. http://dx.doi.org/10.1152/ajpregu.1990.259.5.r1012.

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We examined the salt sensitivity of blood pressure in angiotensin II (ANG II)-induced hypertension. Wistar rats, salt loaded (0.66, 2, or 8% salt-containing diet) for 4 or 12 days, were infused intravenously with 15 or 60 ng/min of ANG II. Systolic blood pressure (SBP) was not increased by long-term (12 days) salt loading, and SBP was unchanged with ANG II and normal-salt (0.66%) diet. However, when combined with salt loading, ANG II produced hypertension in a dose-dependent fashion; compared with control (120 +/- 2 mmHg), SBP was increased with 15 ng/min of ANG II and 8% salt diet (145 +/- 5 mmHg, P less than 0.05) and with 60 ng/min of ANG II and either 2 or 8% salt diet (149 +/- 8 and 174 +/- 8 mmHg, P less than 0.05, respectively). Na space (exchangeable Na) was increased in a roughly similar pattern and correlated significantly (r = 0.531, P less than 0.05) with SBP. However, with 15 ng/min of ANG II, Na space was not different among rats on either level of salt loading, although the 8% salt diet elevated SBP. Data obtained with short-term (4 days) treatment indicate that an elevated Na space preceded development of hypertension. With 15 ng/min of ANG II and 8% salt diet for 4 days, Na space was markedly (P less than 0.05) increased, but SBP was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

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Sasser, Jennifer M., Jennifer S. Pollock, and David M. Pollock. "Renal endothelin in chronic angiotensin II hypertension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 1 (July 1, 2002): R243—R248. http://dx.doi.org/10.1152/ajpregu.00086.2002.

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To determine the influence of chronic ANG II infusion on urinary, plasma, and renal tissue levels of immunoreactive endothelin (ET), ANG II (65 ng/min) or saline vehicle was delivered via osmotic minipump in male Sprague-Dawley rats given either a high-salt diet (10% NaCl) or normal-salt diet (0.8% NaCl). High-salt diet alone caused a slight but not statistically significant increase (7 ± 1%) in mean arterial pressure (MAP). MAP was significantly increased in ANG II-infused rats (41 ± 10%), and the increase in MAP was significantly greater in ANG II rats given a high-salt diet (59 ± 1%) compared with the increase observed in rats given a high-salt diet alone or ANG II infusion and normal-salt diet. After a 2-wk treatment, urinary excretion of immunoreactive ET was significantly increased by ∼50% in ANG II-infused animals and by over 250% in rats on high-salt diet, with or without ANG II infusion. ANG II infusion combined with high-salt diet significantly increased immunoreactive ET content in the cortex and outer medulla, but this effect was not observed in other groups. In contrast, high-salt diet, with or without ANG II infusion, significantly decreased immunoreactive ET content within the inner medulla. These data indicate that chronic elevations in ANG II levels and sodium intake differentially affect ET levels within the kidney and provide further support for the hypothesis that the hypertensive effects of ANG II may be due to interaction with the renal ET system.

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10

SMITH, R. J. "U.S. Official Defends SALT II Decision." Science 232, no. 4756 (June 13, 1986): 1334. http://dx.doi.org/10.1126/science.232.4756.1334.

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11

Smith, R. Jeffrey. "U.S. Official Defends SALT II Decision." Science 232, no. 4756 (June 13, 1986): 1334. http://dx.doi.org/10.1126/science.232.4756.1334.a.

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12

Gutkind, J. S., M. Kurihara, and J. M. Saavedra. "Increased angiotensin II receptors in brain nuclei of DOCA-salt hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (September 1, 1988): H646—H650. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h646.

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We analyzed angiotensin II (ANG II) receptors by in vitro autoradiography in selective brain nuclei of control, salt-treated (1% NaCl in drinking water), deoxycorticosterone acetate (DOCA)-treated (DOCA pivalate, 25 mg/kg sc weekly), and DOCA-salt-treated (DOCA + salt treatments) uninephrectomized male Wistar-Kyoto rats. After 4 wk of treatment, only the DOCA-salt group developed hypertension. ANG II binding increased in median preoptic nucleus and subfornical organ of salt- and DOCA-treated rats. DOCA-treated rats also showed increased ANG II binding in paraventricular nucleus. DOCA-salt-treated rats showed higher ANG II binding in nucleus of the solitary tract and area postrema, as well as in the areas mentioned before. Although salt and/or DOCA treatments alone increased ANG II receptors in some brain nuclei, after combined DOCA-salt treatment there was significantly higher ANG II binding in all areas, except the median preoptic nucleus. These results suggest that increased ANG II receptors in selected brain areas may play a role in the pathophysiology of mineralocorticoid-salt experimental hypertension.

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13

Rudd, M. Audrey, George Toolan, Maria R. Trolliet, Timothy Cloutier, Karlene Maitland, and Joseph Loscalzo. "Short-Term NOS II Inhibition Leads to Long-Term Salt-Sensitivity in Dahl Salt-Resistant Rats." Hypertension 36, suppl_1 (October 2000): 713. http://dx.doi.org/10.1161/hyp.36.suppl_1.713-b.

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P111 We have previously shown that inhibition of inducible nitric oxide synthase (NOS II) evokes a salt-sensitive increase in blood pressure in Dahl salt-resistant rats when given a high salt (8% NaCl) diet for 7 days. To determine whether or not the effect of NOS II inhibition is short-lived, we continued the high salt diet for an additional 3 weeks following the discontinuation of the NOS II inhibitor. DR rats were given one of two NOS II selective inhibitors, AMT (300 nmoles/hr) and 1400W (35 nmoles/hr) for 2 weeks. A high salt diet was initiated after the first week of NOS II inhibition and continued for an additional 3 weeks for a total of 4 weeks of high salt treatment. Control DR rats received high salt alone for 4 weeks. Systolic blood pressure was taken at baseline and once weekly for the treatment period. Blood pressure significantly increased in DR rats after 1 week of high salt following NOS II inhibition. The blood pressure remained elevated throughout the 4-week period of high salt treatment despite the discontinuation of NOS II inhibitors 1 week following the initiation of the high salt diet. There was no significant change in blood pressure in DR rats on high salt diet alone. These data suggest that salt-sensitive hypertension can be evoked by transient NOS II inhibitor exposure. We conclude that tranisent NOS II inhibition may initiate events or processes that high salt maintains leading to sustained elevation in systolic blood pressure.

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14

Lu, Jiao, Hong-Wei Wang, Monir Ahmad, Marzieh Keshtkar-Jahromi, Mordecai P. Blaustein, John M. Hamlyn, and Frans H. H. Leenen. "Central and peripheral slow-pressor mechanisms contributing to Angiotensin II-salt hypertension in rats." Cardiovascular Research 114, no. 2 (November 8, 2017): 233–46. http://dx.doi.org/10.1093/cvr/cvx214.

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AbstractAimsHigh salt intake markedly enhances hypertension induced by angiotensin II (Ang II). We explored central and peripheral slow-pressor mechanisms which may be activated by Ang II and salt.Methods and resultsIn protocol I, Wistar rats were infused subcutaneously with low-dose Ang II (150 ng/kg/min) and fed regular (0.4%) or high salt (2%) diet for 14 days. In protocol II, Ang II-high salt was combined with intracerebroventricular infusion of mineralocorticoid receptor (MR) blockers (eplerenone, spironolactone), epithelial sodium channel (ENaC) blocker (benzamil), angiotensin II type 1 receptor (AT1R) blocker (losartan) or vehicles. Ang II alone raised mean arterial pressure (MAP) ∼10 mmHg, but Ang II-high salt increased MAP ∼50 mmHg. Ang II-high salt elevated plasma corticosterone, aldosterone and endogenous ouabain but not Ang II alone. Both Ang II alone and Ang II-high salt increased mRNA and protein expression of CYP11B2 (aldosterone synthase gene) in the adrenal cortex but not of CYP11B1 (11-β-hydroxylase gene). In the aorta, Ang II-high salt increased sodium-calcium exchanger-1 (NCX1) protein. The Ang II-high salt induced increase in MAP was largely prevented by central infusion of MR blockers, benzamil or losartan. Central blockades significantly lowered plasma aldosterone and endogenous ouabain and markedly decreased Ang II-high salt induced CYP11B2 mRNA expression in the adrenal cortex and NCX1 protein in the aorta.ConclusionThese results suggest that in Ang II-high salt hypertension, MR-ENaC-AT1R signalling in the brain increases circulating aldosterone and endogenous ouabain, and arterial NCX1. These factors can amplify blood pressure responses to centrally-induced sympatho-excitation and thereby contribute to severe hypertension.

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15

Ingert, Catherine, Michèle Grima, Catherine Coquard, Mariette Barthelmebs, and Jean-Louis Imbs. "Contribution of angiotensin II internalization to intrarenal angiotensin II levels in rats." American Journal of Physiology-Renal Physiology 283, no. 5 (November 1, 2002): F1003—F1010. http://dx.doi.org/10.1152/ajprenal.00322.2001.

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This study was designed to determine the involvement of AT1 receptors in the uptake of ANG II in the kidney of rats exposed to differing salt intake. Male Wistar-Kyoto rats were treated with a normal-salt (NS; 1% NaCl, n = 7) or a low-salt (LS; 0.025% NaCl, n = 7) diet combined with (LS+Los, n = 7; NS+Los, n = 7) or without losartan (30 mg · kg−1 · day−1), an AT1 receptor antagonist. Renin (RA) and angiotensin-converting enzyme (ACE) activities and angiotensinogen, ANG I, and ANG II levels were measured in plasma, renal cortex, and medulla. In LS rats, in both plasma and renal cortex, the increase in RA was associated with an increase in ANG I and ANG II levels compared with NS rats, but intrarenal ANG II levels increased more than ANG I levels. In NS+Los rats, the increase in RA in plasma was followed by a marked increase in plasma ANG I and ANG II levels compared with NS rats whereas in the kidney the increase of renal RA was followed by a decrease of the levels of these peptides. The same pattern was observed in LS+Los rats, but the decrease in renal ANG II levels was much more pronounced in LS+Los rats than in NS+Los rats. Our results suggest that the increase in renal ANG II levels after salt restriction results mainly from an uptake of ANG II, via AT1 receptors. Such elevated intrarenal ANG II levels could contribute to maintain sodium and fluid balance and arterial blood pressure during salt-deficiency states.

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16

Nathan, R. J., and L. B. Mudgway. "Estimating Salt Loads in High Water Table Areas. II: Regional Salt Loads." Journal of Irrigation and Drainage Engineering 123, no. 2 (March 1997): 91–99. http://dx.doi.org/10.1061/(asce)0733-9437(1997)123:2(91).

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17

Fitts, Douglas A., Elizabeth M. Starbuck, and Alexandra Ruhf. "Circumventricular organs and ANG II-induced salt appetite: blood pressure and connectivity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2277—R2286. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2277.

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A lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on ANG II, and yet ANG II infusions directly into SFO do not provoke salt appetite. Two experiments were designed to address this apparent contradiction. In experiment 1 sustained infusions of ANG II into SFO did not produce a sustained elevation of blood pressure, and neither a reduction of blood pressure alone with minoxidil and captopril nor a reduction of both blood pressure and volume with furosemide and captopril enhanced salt appetite. Infusions of ANG II in the organum vasculosum laminae terminalis (OVLT) did evoke salt appetite without raising blood pressure. In experiment 2 knife cuts of the afferent and efferent fibers of the rostroventral pole of the SFO abolished water intake during an infusion of ANG II into the femoral vein but failed to reduce salt appetite during an infusion of ANG II into the OVLT. We conclude that 1) hypertension does not account for the failure of infusions of ANG II in the SFO to generate salt appetite and 2) the OVLT does not depend on its connectivity with the SFO to generate salt appetite during ANG II infusions.

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Uijl, Estrellita, Liwei Ren, Katrina M. Mirabito Colafella, Richard van Veghel, Ingrid M. Garrelds, Oliver Domenig, Marko Poglitsch, et al. "No evidence for brain renin–angiotensin system activation during DOCA-salt hypertension." Clinical Science 135, no. 2 (January 2021): 259–74. http://dx.doi.org/10.1042/cs20201239.

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Abstract Brain renin–angiotensin system (RAS) activation is thought to mediate deoxycorticosterone acetate (DOCA)-salt hypertension, an animal model for human primary hyperaldosteronism. Here, we determined whether brainstem angiotensin II is generated from locally synthesized angiotensinogen and mediates DOCA-salt hypertension. To this end, chronic DOCA-salt-hypertensive rats were treated with liver-directed siRNA targeted to angiotensinogen, the angiotensin II type 1 receptor antagonist valsartan, or the mineralocorticoid receptor antagonist spironolactone (n = 6–8/group). We quantified circulating angiotensinogen and renin by enzyme-kinetic assay, tissue angiotensinogen by Western blotting, and angiotensin metabolites by LC-MS/MS. In rats without DOCA-salt, circulating angiotensin II was detected in all rats, whereas brainstem angiotensin II was detected in 5 out of 7 rats. DOCA-salt increased mean arterial pressure by 19 ± 1 mmHg and suppressed circulating renin and angiotensin II by >90%, while brainstem angiotensin II became undetectable in 5 out of 7 rats (<6 fmol/g). Gene silencing of liver angiotensinogen using siRNA lowered circulating angiotensinogen by 97 ± 0.3%, and made brainstem angiotensin II undetectable in all rats (P<0.05 vs. non-DOCA-salt), although brainstem angiotensinogen remained intact. As expected for this model, neither siRNA nor valsartan attenuated the hypertensive response to DOCA-salt, whereas spironolactone normalized blood pressure and restored brain angiotensin II together with circulating renin and angiotensin II. In conclusion, despite local synthesis of angiotensinogen in the brain, brain angiotensin II depended on circulating angiotensinogen. That DOCA-salt suppressed circulating and brain angiotensin II in parallel, while spironolactone simultaneously increased brain angiotensin II and lowered blood pressure, indicates that DOCA-salt hypertension is not mediated by brain RAS activation.

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Wilson, John X. "Adrenergic and osmotic responses to atrial natriuretic peptide and angiotensin II in the duck (Anas platyrhynchos)." Canadian Journal of Physiology and Pharmacology 65, no. 9 (September 1, 1987): 1995–99. http://dx.doi.org/10.1139/y87-311.

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There is evidence that analogues of atrial natriuretic peptide (ANP) and angiotensin II (ANG II) occur in birds. The present experiments studied the adrenergic and osmoregulatory responses to synthetic ANP and ANG II in salt-loaded ducks (Anas platyrhynchos). Excretion of water and salt through the nasal salt glands was abolished by ANG II. This extrarenal, salt-retaining effect of ANG II was not altered by ANP. However, ANP did augment the diuretic response to ANG II. ANP also potentiated the stimulatory effect of ANG II on plasma norepinephrine. The data are consistent with physiological roles for native analogues of ANP and ANG II in adrenergic and osmotic regulation in the duck.

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Gilfedder, Mathew, Russell G. Mein, and Luke D. Connell. "Border Irrigation Field Experiment. II: Salt Transport." Journal of Irrigation and Drainage Engineering 126, no. 2 (March 2000): 92–97. http://dx.doi.org/10.1061/(asce)0733-9437(2000)126:2(92).

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21

Peruzzo, Mattia, Gregorio P. Milani, Luca Garzoni, Laura Longoni, Giacomo D. Simonetti, Alberto Bettinelli, Emilio F. Fossali, and Mario G. Bianchetti. "Body fluids and salt metabolism - Part II." Italian Journal of Pediatrics 36, no. 1 (2010): 78. http://dx.doi.org/10.1186/1824-7288-36-78.

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22

Biais, J., M. Barthe, M. Bourrel, B. Clin, and P. Lalanne. "Salt partitioning in Winsor Type II systems." Journal of Colloid and Interface Science 109, no. 2 (February 1986): 576–85. http://dx.doi.org/10.1016/0021-9797(86)90339-5.

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Valenza, John J., and George W. Scherer. "A review of salt scaling: II. Mechanisms." Cement and Concrete Research 37, no. 7 (July 2007): 1022–34. http://dx.doi.org/10.1016/j.cemconres.2007.03.003.

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24

Shao, Weijian, Dale M. Seth, Minolfa C. Prieto, Hiroyuki Kobori, and L. Gabriel Navar. "Activation of the renin-angiotensin system by a low-salt diet does not augment intratubular angiotensinogen and angiotensin II in rats." American Journal of Physiology-Renal Physiology 304, no. 5 (March 1, 2013): F505—F514. http://dx.doi.org/10.1152/ajprenal.00587.2012.

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In angiotensin II (ANG II) infusion hypertension, there is an augmentation of intratubular angiotensinogen (AGT) and ANG II leading to increased urinary AGT and ANG II excretion rates associated with tissue injury. However, the changes in urinary AGT and ANG II excretion rates and markers of renal injury during physiologically induced stimulation of the renin-angiotensin system (RAS) by a low-salt diet remain unclear. Male Sprague-Dawley rats received a low-salt diet (0.03% NaCl; n = 6) and normal-salt diet (0.3% NaCl, n = 6) for 13 days. Low-salt diet rats had markedly higher plasma renin activity and plasma ANG II levels. Kidney cortex renin mRNA, kidney AGT mRNA, and AGT immunoreactivity were not different; however, medullary renin mRNA, kidney renin content, and kidney ANG II levels were significantly elevated by the low-salt diet. Kidney renin immunoreactivity was also markedly increased in juxtaglomerular apparati and in cortical and medullary collecting ducts. Urinary AGT excretion rates and urinary ANG II excretion rates were not augmented by the low-salt diet. The low-salt diet caused mild renal fibrosis in glomeruli and the tubulointerstitium, but no other signs of kidney injury were evident. These results indicate that, in contrast to the response in ANG II infusion hypertension, the elevated plasma and intrarenal ANG II levels caused by physiological stimulation of RAS are not reflected by increased urinary AGT or ANG II excretion rates or the development of renal injury.

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Bezanilla, Magdalena, and Thomas D. Pollard. "Myosin-II Tails Confer Unique Functions inSchizosaccharomyces pombe: Characterization of a Novel Myosin-II Tail." Molecular Biology of the Cell 11, no. 1 (January 2000): 79–91. http://dx.doi.org/10.1091/mbc.11.1.79.

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Schizosaccharomyces pombe has two myosin-IIs, Myo2p and Myp2p, which both concentrate in the cleavage furrow during cytokinesis. We studied the phenotype of mutant myosin-II strains to examine whether these myosins have overlapping functions in the cell.myo2 + is essential.myp2 + cannot rescue loss ofmyo2 + even at elevated levels of expression.myp2 + is required under specific nutritional conditions; thus myo2 + cannot rescue under these conditions. Studies with chimeras show that the tails rather than the structurally similar heads determine the gene-specific functions ofmyp2 + and myo2 +. The Myo2p tail is a rod-shaped coiled-coil dimer that aggregates in low salt like other myosin-II tails. The Myp2p tail is monomeric in high salt and is insoluble in low salt. Biophysical properties of the full-length Myp2p tail and smaller subdomains indicate that two predicted coiled-coil regions fold back on themselves to form a rod-shaped antiparallel coiled coil. This suggests that Myp2p is the first type II myosin with only one head. The C-terminal two-thirds of Myp2p tail are essential for function in vivo and may interact with components of the salt response pathway.

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Bouhnik, J., J. P. Richoux, H. Huang, F. Savoie, T. Baussant, F. Alhenc-Gelas, and P. Corvol. "Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies." Clinical Science 83, no. 1 (July 1, 1992): 13–22. http://dx.doi.org/10.1042/cs0830013.

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1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.

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Ballew, Jennifer R., and Gregory D. Fink. "Role of endothelin ETB receptor activation in angiotensin II-induced hypertension: effects of salt intake." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 5 (November 1, 2001): H2218—H2225. http://dx.doi.org/10.1152/ajpheart.2001.281.5.h2218.

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We showed recently that endothelin (ET)A receptors are involved in the salt sensitivity of ANG II-induced hypertension. The objective of this current study was to characterize the role of endothelin ETB receptor activation in the same model. Male rats on fixed normal (2 meq/day) or high (6 meq/day) salt intake received a continuous intravenous infusion of ANG II or salt only for 15 days. During the middle 5 days of the infusion period, rats were given either the selective ETB receptor antagonist A-192621 or the nonselective endothelin receptor antagonist A-182086 (both at 24 mg · kg−1 · day−1intra-arterially). Infusion of ANG II caused a greater rise in arterial pressure in rats on high-salt intake. The administration of A-192621 increased arterial pressure further in all rats. The chronic hypertensive effect of A-192621 was not significantly affected by salt intake or ANG II. The administration of A-182086 lowered arterial pressure chronically only in rats on normal salt intake receiving ANG II. Thus the salt sensitivity of ANG II-induced hypertension is not caused by changes in ETB receptor function.

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Toscano, Stefania, Giovanni La Fornara, and Daniela Romano. "Salt Spray and Surfactants Induced Morphological, Physiological, and Biochemical Responses in Callistemon citrinus (Curtis) Plants." Horticulturae 8, no. 3 (March 17, 2022): 261. http://dx.doi.org/10.3390/horticulturae8030261.

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The growth and aesthetic value of ornamental plant species used near coastlines are negatively influenced by salt spray. The presence of surfactants could enhance salt damage. To analyze the influences of salt spray and surfactants alone and in combination with each other, individual Callistemon plants were subjected to different treatments for 8 weeks: a solution simulating the composition of seawater (salt spray), a solution containing an anionic surfactant (surfactant), a solution with salt spray and anionic surfactant (salt plus surfactants), and deionized water (control). To study the influence of different climatic conditions, two growing periods, from January to March (I CP) and from May to July (II CP), were established. Salt spray, alone or with surfactant action, influences plants’ growth and aesthetic features in different cycle periods. The percentage of leaf damage significantly increased with salt spray and salt plus surfactants during II CP (~27%). Additionally, the Na+ and Cl− contents were enhanced in the leaves in both CPs, but the contents in the roots were only enhanced in the II CP. The gas exchanges were significantly influenced by the treatments, especially during the II CP, when a reduction in net photosynthesis due to salt spray was observed starting from the second week of stress. At the end of the experiment, in both cycle periods, the leaf proline content increased in the salt spray and salt plus surfactants treatments. In both CPs, PCA revealed that the morphological and physiological parameters were directly associated with the control and surfactants treatments, whereas the mineral contents and biochemical parameters were directly correlated with the salt and salt plus surfactants treatments. The additive effect of surfactant stress, compared to salt stress, did not appear to be significant, with the exception of CP II, and for some parameters, the solubilization action of surfactants was favored by higher temperatures.

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Zuo, Zhiyu, Junhong Guo, Caiyun Xin, Shengqun Liu, Hanping Mao, Yongjun Wang, and Xiangnan Li. "Salt acclimation induced salt tolerance in wild-type and abscisic acid-deficient mutant barley." Plant, Soil and Environment 65, No. 10 (November 5, 2019): 516–21. http://dx.doi.org/10.17221/506/2019-pse.

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Salt acclimation is a process to enhance salt tolerance in plants. The salt acclimation induced salt tolerance was investigated in a spring barley (Hordeum vulgare L.) cv. Steptoe (wild type, WT) and its abscisic acid (ABA)-deficient mutant Az34. Endogenesis ABA concentration in leaf was significantly increased by salt stress in WT, while it was not affected in Az34. Under salt stress, the salt acclimated Az34 plants had 14.8% lower total soluble sugar concentration and 93.7% higher sodium (Na) concentration in leaf, compared with salt acclimated WT plants. The acclimated plants had significantly higher leaf water potential and osmotic potential than non-acclimated plants in both WT and Az34 under salt stress. The salt acclimation enhanced the net photosynthetic rate (by 22.9% and 12.3%) and the maximum quantum yield of PS II (22.7% and 22.0%) in WT and Az34 under salt stress. However, the stomatal conductance in salt acclimated Az34 plants was 28.9% lower than WT under salt stress. Besides, the guard cell pair width was significantly higher in salt acclimated Az34 plants than that in WT plants. The results indicated that the salt acclimated WT plants showed a higher salt tolerance than Az34 plants, suggesting that ABA deficiency has a negative effect on the salt acclimation induced salt tolerance in barley.

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Franco, Martha, Flavio Martínez, Bernardo Rodríguez-Iturbe, Richard J. Johnson, José Santamaría, Angélica Montoya, Tomas Nepomuceno, Rocío Bautista, Edilia Tapia, and Jaime Herrera-Acosta. "Angiotensin II, interstitial inflammation, and the pathogenesis of salt-sensitive hypertension." American Journal of Physiology-Renal Physiology 291, no. 6 (December 2006): F1281—F1287. http://dx.doi.org/10.1152/ajprenal.00221.2006.

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Transient administration of ANG II causes persistent salt-sensitive hypertension associated with arteriolopathy, interstitial inflammation, and cortical vasoconstriction; blocking the vascular and inflammatory changes with mycophenolate mofetil (MMF) prevents vasoconstriction. While infiltrating leukocytes during the salt-sensitive hypertension phase express ANG II, the functional role of ANG II during this phase is not known. We examined the acute effect of candesartan on renal hemodynamics during the established salt-sensitive hypertensive phase and related these findings to direct measurement of intrarenal ANG II and inflammatory cells in rats previously exposed to ANG II with or without MMF treatment. Sham controls were also examined. The administration of ANG II, followed by exposure to high-salt diet, resulted in hypertension, cortical vasoconstriction, an increase in interstitial inflammatory cells (44.8 ± 1.3 lymphocytes/mm2, and 30.8 ± 1.2 macrophages/mm2 ANG II vs. 19.6 ± 2 lymphocytes/mm2, and 22 ± 0.7 macrophages/mm2 Sham), and increase in renal ANG II levels (1,358 ± 74.6 pg/ml ANG II vs. 194 ± 9.28 pg/ml Sham). Treatment with MMF during the administration of exogenous ANG II resulted in reduction in renal interstitial inflammation (19.7 ± 0.9 lymphocytes/mm2 and 15.9 ± 0.8 machophages/mm2), ANG II levels (436.9 ± 52.29 pg/ml), cortical vasoconstriction, and stable blood pressure levels during the subsequent challenge with a high-salt diet. Acute administration of candesartan similarly reduced renal vasoconstriction and blood pressure. We conclude that the cortical vasoconstriction occurring with salt-sensitive hypertension following exposure to ANG II is mediated by intrarenal ANG II, related, at least in part, to the interstitial inflammation.

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Clemmer, John S., W. Andrew Pruett, Thomas G. Coleman, John E. Hall, and Robert L. Hester. "Mechanisms of blood pressure salt sensitivity: new insights from mathematical modeling." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 312, no. 4 (April 1, 2017): R451—R466. http://dx.doi.org/10.1152/ajpregu.00353.2016.

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Mathematical modeling is an important tool for understanding quantitative relationships among components of complex physiological systems and for testing competing hypotheses. We used HumMod, a large physiological model, to test hypotheses of blood pressure (BP) salt sensitivity. Systemic hemodynamics, renal, and neurohormonal responses to chronic changes in salt intake were examined during normal renal function, fixed low or high plasma angiotensin II (ANG II) levels, bilateral renal artery stenosis, increased renal sympathetic nerve activity (RSNA), and decreased nephron numbers. Simulations were run for 4 wk at salt intakes ranging from 30 to 1,000 mmol/day. Reducing functional kidney mass or fixing ANG II increased salt sensitivity. Salt sensitivity, associated with inability of ANG II to respond to changes in salt intake, occurred with smaller changes in renal blood flow but greater changes in glomerular filtration rate, renal sodium reabsorption, and total peripheral resistance (TPR). However, clamping TPR at normal or high levels had no major effect on salt sensitivity. There were no clear relationships between BP salt sensitivity and renal vascular resistance or extracellular fluid volume. Our robust mathematical model of cardiovascular, renal, endocrine, and sympathetic nervous system physiology supports the hypothesis that specific types of kidney dysfunction, associated with impaired regulation of ANG II or increased tubular sodium reabsorption, contribute to BP salt sensitivity. However, increased preglomerular resistance, increased RSNA, or inability to decrease TPR does not appear to influence salt sensitivity. This model provides a platform for testing competing concepts of long-term BP control during changes in salt intake.

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Zammit, Carla M., L. A. Mutch, Helen R. Watling, and Elizabeth L. J. Watkin. "The Characterization of Salt Tolerance in Biomining Microorganisms and the Search for Novel Salt Tolerant Strains." Advanced Materials Research 71-73 (May 2009): 283–86. http://dx.doi.org/10.4028/www.scientific.net/amr.71-73.283.

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In this study an acidic saline drain in the Western Australian wheat belt was sampled and enriched for salt tolerant chemolithotrophic microorganisms in acidic media containing up to 100 gL-1 NaCl. A mixed consortium was obtained which grows at pH 1.8 and oxidises iron (II) in the presence of up to 30 gL-1 NaCl. In comparative tests (growth rates and iron (II) oxidation rates) it was found that NaCl concentrations >3.5 gL-1 generally cause reduced growth and iron (II) oxidation rates in known biomining organisms. The results help to set a benchmark for NaCl tolerance in known biomining microorganisms and will lead to the generation of a consortium of microorganisms that can oxidise iron (II) effectively in saline process water.

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Lu, Congming, and Jianhua Zhang. "Thermostability of photosystem II is increased in salt-stressed sorghum." Functional Plant Biology 25, no. 3 (1998): 317. http://dx.doi.org/10.1071/pp97138.

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Modulated chlorophyll fluorescence and rapid fluorescence induction kinetics were used to evaluate the functions of photosystem II (PSII) photochemsitry in sorghum leaves exposed to salinity (0–100 mM NaCl) and/or high temperature stress (30–50°C). No differences were detected in the steady- state fluorescence parameters and rapid fluorescence induction kinetics in salt-stressed leaves, indicating that PSII was highly resistant to salinity stress alone. However, salinity stress modified the responses of PSII to high temperature. When the temperature was above 45°C, the thermostability of PSII was strongly enhanced in salt-stressed leaves, which was reflected in a smaller decrease in maximum efficiency of PSII photochemistry, coefficients of photochemical and non-photochemical quenching, and efficiency of excitation capture by open PSII reaction centres, and in a smaller increase in the proportion of the QB-non-reducing PSII centres in salt-stressed leaves than in control leaves. This increased thermostability in salt-stressed leaves exposed to high temperature seemed to be independent of the imposed salt concentration since there were no significant variations in the above fluorescence parameters among the salt-stressed plants treated with different salt concentrations. The results are discussed in terms of the physiological significance of such increased resistance of PSII to high temperature.

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Larson, Robert A., Le Gui, Michael J. Huber, Andrew D. Chapp, Jianhua Zhu, Lila P. LaGrange, Zhiying Shan, and Qing-Hui Chen. "Sympathoexcitation in ANG II-salt hypertension involves reduced SK channel function in the hypothalamic paraventricular nucleus." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 12 (June 15, 2015): H1547—H1555. http://dx.doi.org/10.1152/ajpheart.00832.2014.

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Hypertension (HTN) resulting from subcutaneous infusion of ANG II and dietary high salt (HS) intake involves sympathoexcitation. Recently, we reported reduced small-conductance Ca2+-activated K+ (SK) current and increased excitability of presympathetic neurons in the paraventricular nucleus (PVN) in ANG II-salt HTN. Here, we hypothesized that ANG II-salt HTN would be accompanied by altered PVN SK channel activity, which may contribute to sympathoexcitation in vivo. In anesthetized rats with normal salt (NS) intake, bilateral PVN microinjection of apamin (12.5 pmol/50 nl each), the SK channel blocker, remarkably elevated splanchnic sympathetic nerve activity (SSNA), renal sympathetic nerve activity (RSNA), and mean arterial pressure (MAP). In contrast, rats with ANG II-salt HTN demonstrated significantly attenuated SSNA, RSNA, and MAP ( P < 0.05) responses to PVN-injected apamin compared with NS control rats. Next, we sought to examine the individual contributions of HS and subcutaneous infusion of ANG II on PVN SK channel function. SSNA, RSNA, and MAP responses to PVN-injected apamin in rats with HS alone were significantly attenuated compared with NS-fed rats. In contrast, sympathetic nerve activity responses to PVN-injected apamin in ANG II-treated rats were slightly attenuated with SSNA, demonstrating no statistical difference compared with NS-fed rats, whereas MAP responses to PVN-injected apamin were similar to NS-fed rats. Finally, Western blot analysis showed no statistical difference in SK1–SK3 expression in the PVN between NS and ANG II-salt HTN. We conclude that reduced SK channel function in the PVN is involved in the sympathoexcitation associated with ANG II-salt HTN. Dietary HS may play a dominant role in reducing SK channel function, thus contributing to sympathoexcitation in ANG II-salt HTN.

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Thompson, C. I., and A. N. Epstein. "Salt appetite in rat pups: ontogeny of angiotensin II-aldosterone synergy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 2 (February 1, 1991): R421—R429. http://dx.doi.org/10.1152/ajpregu.1991.260.2.r421.

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Preweanling rats were tested to determine whether angiotensin II (ANG II) and aldosterone (Aldo) act synergistically to enhance salt appetite at 12 and 17 days. Twelve-day-old pups received one of four hormone treatments in four doses: 1) ANG II only [1, 2, 10, or 100 ng pulse intracerebroventricular (icv)], 2) Aldo only (1, 2, 10, or 40 micrograms/day sc), 3) Aldo + ANG II (four individual doses combined), or 4) vehicle. Seventeen-day-old rats received the same treatments in two doses (2 or 100 ng ANG II; 2 or 40 micrograms Aldo). Pups were presatiated with milk through anterior oral catheters and then given either 4% NaCl or water for 30 min. Intake was assessed by body weight change. At both ages, ANG II enhanced salt (and water) intake, and Aldo enhanced salt (but not water) intake. Minimum effective doses were comparable to those reported for adults. ANG II-Aldo synergy was absent at 12 days and present at 17 days, when salt intake was 590% greater than the summed intakes evoked by ANG II and Aldo alone. The neural mechanisms for ANG II-Aldo synergy thus mature later than those mediating the hormone's individual actions in arousing salt appetite.

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Asirvatham-Jeyaraj, Ninitha, Andrew J. King, Carrie A. Northcott, Shivanshu Madan, and Gregory D. Fink. "Cyclooxygenase-1 inhibition attenuates angiotensin II-salt hypertension and neurogenic pressor activity in the rat." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 10 (November 15, 2013): H1462—H1470. http://dx.doi.org/10.1152/ajpheart.00245.2013.

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Cyclooxygenase (COX)-derived prostanoids contribute to angiotensin II (ANG II) hypertension (HTN). However, the specific mechanisms by which prostanoids act are unclear. ANG II-induced HTN is caused partly by increased sympathetic nervous system activity, especially in a setting of high dietary salt intake. This study tested the hypothesis that COX-derived prostanoids cause ANG II-salt sympathoexcitation and HTN. Experiments were conducted in conscious rats. Infusion of ANG II (150 ng·kg−1·min−1 sc) caused a marked HTN in rats on 2% salt diet, but a much smaller increase in blood pressure in rats on 0.4% salt diet. The nonselective COX inhibitor ketoprofen (2 mg/kg sc) given throughout the ANG-II infusion period attenuated HTN development in rats on 2% NaCl diet, but not in rats on 0.4% NaCl diet. The acute depressor response to ganglion blockade was used to assess neurogenic pressor activity in rats on 2% NaCl diet. Ketoprofen-treated rats showed a smaller fall in arterial pressure in response to ganglion blockade during ANG-II infusion than did nontreated controls. In additional experiments, ketoprofen-treated rats exhibited smaller increases in plasma norepinephrine levels and whole body norepinephrine spillover than we previously reported in ANG II-salt HTN. Finally, the effects of the selective COX-1 inhibitor SC560 (10 mg·kg−1·day−1 ip) and the selective COX-2 inhibitor nimesulide (10 mg·kg−1·day−1 ip) were investigated. Treatment with SC560 but not nimesulide significantly reduced blood pressure and the depressor response to ganglion blockade in ANG II-salt HTN rats. The results suggest that COX-1 products are critical for sympathoexcitation and the full development of ANG II-salt HTN in rats.

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Sekacis, Ilmars, Mark Shenderovich, Gregory Nikiforovich, Edvards Liepinš, Ludmila Polevaya, and Gunars Chipens. "Salt bridges in model peptides." Collection of Czechoslovak Chemical Communications 53, no. 11 (1988): 2810–24. http://dx.doi.org/10.1135/cccc19882810.

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A group of synthetic peptides including Boc-Lys-Phe-X-Y, X = Ala (I, III) or Thr (II), Y = Pro (I, II) or Ala (III) was studied by means of 1H NMR spectroscopy and theoretical conformational analysis. Compound I in DMSO shows two conformers with the trans- and cis-configuration of the peptide bond Ala-Pro. The salt bridge between the Lys ε-amino group and the C-terminal carboxyl is featured by magnetic nonequivalence of the Lys CεH2 protons. The space structure of I and II was found to possess a salt bridge fixed by an unusual turn in the chain formed by the Lys side chain and the C-terminal dipeptide with the trans-peptide bond X-Pro. Since a stable ionic bond in III and in the cis-conformer of I has not been observed, its contribution to stabilization of the space structure of the peptides in DMSO appears rather small.

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Huang, Bing S., Roselyn A. White, Li Bi, and Frans H. H. Leenen. "Central infusion of aliskiren prevents sympathetic hyperactivity and hypertension in Dahl salt-sensitive rats on high salt intake." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 7 (April 1, 2012): R825—R832. http://dx.doi.org/10.1152/ajpregu.00368.2011.

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Central infusion of an angiotensin type 1 (AT1) receptor blocker prevents sympathetic hyperactivity and hypertension in Dahl salt-sensitive (S) rats on high salt. In the present study, we examined whether central infusion of a direct renin inhibitor exerts similar effects. Intracerebroventricular infusion of aliskiren at the rate of 0.05 mg/day markedly inhibited the increase in ANG II levels in the cerebrospinal fluid and in blood pressure (BP) caused by intracerebroventricular infusion of rat renin. In Dahl S rats on high salt, intracerebroventricular infusion of aliskiren at 0.05 and 0.25 mg/day for 2 wk similarly decreased resting BP in Dahl S rats on high salt. In other groups of Dahl S rats, high salt intake for 2 wk increased resting BP by ∼25 mmHg, enhanced pressor and sympathoexcitatory responses to air-stress, and desensitized arterial baroreflex function. All of these effects were largely prevented by intracerebroventricular infusion of aliskiren at 0.05 mg/day. Aliskiren had no effects in rats on regular salt. Neither high salt nor aliskiren affected hypothalamic ANG II content. These results indicate that intracerebroventricular infusions of aliskiren and an AT1 receptor blocker are similarly effective in preventing salt-induced sympathetic hyperactivity and hypertension in Dahl S rats, suggesting that renin in the brain plays an essential role in the salt-induced hypertension. The absence of an obvious increase in hypothalamic ANG II by high salt, or decrease in ANG II by aliskiren, suggests that tissue levels do not reflect renin-dependent ANG II production in sympathoexcitatory angiotensinergic neurons.

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Petersen, Matthew C., Diane H. Munzenmaier, and Andrew S. Greene. "Angiotensin II infusion restores stimulated angiogenesis in the skeletal muscle of rats on a high-salt diet." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 1 (July 2006): H114—H120. http://dx.doi.org/10.1152/ajpheart.01116.2005.

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Elevated dietary salt intake has previously been demonstrated to have dramatic effects on microvascular structure and function. The purpose of this study was to determine whether a high-salt diet modulates physiological angiogenesis in skeletal muscle. Male Sprague-Dawley rats were placed on a control diet (0.4% NaCl by weight) or a high-salt diet (4.0% NaCl) before implantation of a chronic electrical stimulator. After seven consecutive days of unilateral hindlimb muscle stimulation, animals on control diets demonstrated a significant increase in microvessel density in the tibialis anterior muscle of the stimulated hindlimb relative to the contralateral control leg. High salt-fed rats demonstrated a complete inhibition of this angiogenic response, as well as a significant reduction in plasma ANG II levels compared with those of control animals. To investigate the role of ANG II suppression on the inhibitory effect of high-salt diets, a group of rats that were fed high salt were chronically infused with ANG II at a low dose. Maintenance of ANG II levels restored stimulated angiogenesis to control levels in animals fed a high-salt diet. Western blot analysis indicated that inhibition of angiogenesis in high salt-fed rats was not due to changes in VEGF or VEGF receptor type 1 protein expression in response to stimulation; however, the degree to which VEGF receptor 2 protein increased with stimulation was significantly lower in high salt-fed animals. This study demonstrates an inhibitory effect of high salt intake on stimulated angiogenesis and suggests a critical role for ANG II suppression in mediating this antiangiogenic effect.

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Nurkiewicz, Timothy R., and Matthew A. Boegehold. "Reinforcement of arteriolar myogenic activity by endogenous ANG II: susceptibility to dietary salt." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (July 1, 2000): H269—H278. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h269.

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The purpose of this study was to determine whether endogenous ANG II augments arteriolar myogenic behavior in striated muscle. Because circulating ANG II is decreased during high salt intake, we also investigated whether dietary salt could alter any influence of ANG II on myogenic behavior. Normotensive rats fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated box with the spinotrapezius muscle exteriorized for intravital microscopy. Dietary salt did not affect resting arteriolar diameters. Microvascular pressure elevation by box pressurization caused greater arteriolar constriction in LS rats (up to 12 μm) than in HS rats (up to 4 μm). The ANG II-receptor antagonists saralasin and losartan attenuated myogenic responsiveness in LS rats but not HS rats. The bradykinin-receptor antagonist HOE-140 had no effect on myogenic responsiveness in LS rats but augmented myogenic responsiveness in HS rats. HOE-140 with the angiotensin-converting enzyme inhibitor captopril attenuated myogenic responsiveness to a greater extent in LS rats than in HS rats. We conclude that endogenous ANG II normally reinforces arteriolar myogenic behavior in striated muscle and that attenuated myogenic behavior associated with high salt intake is due to decreased circulating ANG II and increased local kinin levels.

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Heinz, Myriam K., and David A. Gray. "Role of plasma ANG II in the excretion of acute sodium load in a bird with salt glands (Anas platyrhynchos)." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 1 (July 1, 2001): R346—R351. http://dx.doi.org/10.1152/ajpregu.2001.281.1.r346.

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This study was designed to further examine the role of plasma ANG II in the excretion of sodium in the Pekin duck, a bird with salt glands. Renal and extrarenal (salt gland) excretion of an intravenously administered isotonic saline load was monitored over a 4-h period in a group of eight birds under two conditions: the control condition, in which isotonic saline infusion decreased endogenous plasma ANG II from 102.6 to 16.5 pg/ml, and the experimental condition, in which ANG II suppression was prevented by intravenous infusion of a 3.5 ng · kg−1 · min−1 dose of synthetic ANG II. ANG II infusion significantly decreased the total sodium excretion (by 15%), primarily via an inhibition of salt gland output. The results suggest that ANG II suppression facilitates the excretion of an administered sodium load in birds with salt glands.

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Hernandez, I., A. W. Cowley, J. H. Lombard, and A. S. Greene. "Salt intake and angiotensin II alter microvessel density in the cremaster muscle of normal rats." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 3 (September 1, 1992): H664—H667. http://dx.doi.org/10.1152/ajpheart.1992.263.3.h664.

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This study investigated the effect of salt intake and angiotensin II (ANG II) levels on microvessel density (MVD). Rats with indwelling arterial and venous catheters were placed on either a high-salt (HS; 4%) or a low-salt diet (LS; 0.4%) for 2 or 4 wk, and blood pressure, heart rate, and plasma renin activity were measured. Plasma ANG II was fixed at normal levels in half of the rats on HS by continuous intravenous infusion of ANG II (5 ng.kg-1.min-1). Samples of cremaster muscle were examined histologically to determine MVD. No difference in MVD was observed between HS and LS groups after 2 wk. After 4 wk on HS, MVD was reduced (22.4%, P less than 0.05) compared with the LS group. In rats fed HS, ANG II infusion induced a significant dose-dependent increase in MVD from 85.11 +/- 3.34 to 98.94 +/- 4.62 (ANG II, 5 ng.kg-1.min-1) and to 107.60 +/- 7.00 (ANG II, 10 ng.kg-1.min-1) (P less than 0.05), with no change in blood pressure. Maintenance of ANG II levels for 4 wk blocked the rarefaction due to salt. These results suggest that the decrease in MVD due to salt could be the result of a dietary-induced fall in plasma ANG II levels.

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Fitts, D. A., and R. L. Thunhorst. "Rapid elicitation of salt appetite by an intravenous infusion of angiotensin II in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 5 (May 1, 1996): R1092—R1098. http://dx.doi.org/10.1152/ajpregu.1996.270.5.r1092.

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A role for the renal renin-angiotensin system in the direct stimulation of salt appetite in the rat remains controversial because attempts to elicit the behavior by intravenous administration of angiotensin II (ANG II) have been unconvincing. We recently demonstrated that depletion-induced salt appetite was attenuated by selective blockade of peripheral ANG II synthesis with an intravenous dose of converting enzyme inhibitor [captopril (Cap)] that does not block the synthesis of ANG II inside the blood brain barrier. We now show that intravenous ANG II at 30 ng/min rapidly reestablishes salt appetite in Cap-blocked rats. The mean arterial blood pressure (MAP) of unblocked, sodium-depleted rats was normal, but Cap-blocked, depleted rats had low MAP. An intravenous infusion of ANG II in Cap-blocked rats brought MAP into the normal range and elicited water and salt drinking within 90 min. Phenylephrine also normalized MAP but failed to elicit fluid intake in Cap-blocked, sodium-deficient rats. Sodium and water balances tended to be more positive during ANG II than during phenylephrine infusions. Thus circulating ANG II may stimulate both thirst and salt appetite by a direct action on the brain and not by causing natriuresis or by raising the blood pressure.

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Guerra-Doce, Elisa, Germán Delibes de Castro, F. Javier Abarquero-Moras, Jesús M. del Val-Recio, and Ángel L. Palomino-Lázaro. "The Beaker salt production centre of Molino Sanchón II, Zamora, Spain." Antiquity 85, no. 329 (August 2011): 805–18. http://dx.doi.org/10.1017/s0003598x00068320.

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The authors take us to the salt lakes of Villafáfila in north-west Spain, where they have demonstrated by excavation that salt extraction had begun by the second half of the third millennium BC. The salt pans uncovered were accompanied by copious amounts of decorated Beaker pottery, for which political and symbolic interpretations are proposed.

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Grove, Levi J., Allen G. Oliver, Jeanette A. Krause, and William B. Connick. "Structure of a Crystalline Vapochromic Platinum(II) Salt." Inorganic Chemistry 47, no. 5 (March 2008): 1408–10. http://dx.doi.org/10.1021/ic701523e.

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Whittington, Shelly J., and Trevor P. Creamer. "Salt Bridges Do Not Stabilize Polyproline II Helices†." Biochemistry 42, no. 49 (December 2003): 14690–95. http://dx.doi.org/10.1021/bi035565x.

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Jerwood, L. C., D. A. Robinson, and R. B. G. Williams. "Experimental frost and salt weathering of chalk—II." Earth Surface Processes and Landforms 15, no. 8 (December 1990): 699–708. http://dx.doi.org/10.1002/esp.3290150804.

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Mercier, Nicolas, Antoine Seyeux, Celine Morel, and Amedee Riou. "(2-Thienylmethyl)ammonium trichlorostannate(II): a hybrid salt." Acta Crystallographica Section C Crystal Structure Communications 58, no. 2 (January 31, 2002): m127—m128. http://dx.doi.org/10.1107/s0108270101020856.

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Yang, Jun, Stig E. Friberg, Johan Sjöblom, Erkki Paatero, and Satu Sundqist. "Hydrolysis of tetraethoxysilane by copper(II) salt hydrates." Colloids and Surfaces A: Physicochemical and Engineering Aspects 104, no. 2-3 (November 1995): 223–30. http://dx.doi.org/10.1016/0927-7757(95)03281-x.

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Izumi, Hiroshi, and Ikuko Nakamura. "Salt preference elicited by chronic intracerebroventricular angiotensin II." General Pharmacology: The Vascular System 25, no. 6 (October 1994): 1207–12. http://dx.doi.org/10.1016/0306-3623(94)90139-2.

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Journal articles on the topic 'SALT II'

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